March 2024

In this VETgirl online veterinary continuing education blog, Dr. Christopher Kennedy, DACVECC, DECVECC discusses how to assess left ventricular systolic function on Focused Cardiac Ultrasound (FCU) in the dog and cat. In this blog, he will review how to recognize what left ventricular contraction is (or is not) telling us, and how to understand the limitations of the FCU and when the need for a formal echocardiography by a board-certified cardiologist is warranted.

By Dr. Christopher Kennedy, DACVECC, DECVECC

Assessing Left Ventricular Systolic Function on Focused Cardiac Ultrasound

The goals of this blog are:

1. To discuss the contraction of the left ventricle as seen by FCU.
2. To recognise what left ventricular contraction is and is not telling us.
3. To understand limitations of FCU and the need for formal echocardiography by a cardiologist.

This week’s post is a little drier: rather than cool echocardiography images, we are discussing physiology. Specifically, we are considering contraction of the left ventricle (LV) as seen by Focused Cardiac Ultrasound (FCU) and discussing what that means. In the coming weeks, we will explore objective and subjective ways to assess LV systolic function.

Contraction of the LV
The LV is upstream of the aorta and downstream of the left atrium. Its two main roles are to pump blood forward through the aortic valve during systole and to suck blood (forward) into itself through the mitral valve during diastole.(1)  In FCU, we refer to systolic function as the visible contraction of the LV during systole – when the sarcomeres shorten and the lumen volume reduces.(2) Often, it is assumed that the visible reduction in the lumen is a) representative of cardiac performance, b) correlates with the volume of blood ejected from the LV, and c) represents contractility. However, these assumptions may be incorrect.

Left ventricular (LV) performance is the ability to transfer blood into the arteries and is quantified as cardiac output (CO, ml/min).(1)  This is typically what we consider important in critical care: the net output (performance) must meet the metabolic needs (e.g., oxygen demand). The systolic contraction assessed by FCU does not accurately describe cardiac performance: the visible contraction does not accurately describe the stroke volume (SV), so it cannot describe CO.

Inotropy is the force generated by the contracting muscle.(1)  It is influenced by sarcomere length, calcium and the velocity of contraction. FCU considers the change in length (contraction) of the LV as a whole and not the force, so does not accurately describe inotropy. Contractility is different: it is the intrinsic, load and length-independent process responsible for developing force (inotropy) and velocity.(1)  This difference is discussed in reference #1. Contractility can be understood graphically by mapping different Frank-Starling curves (See Figure 1).

Frank Starling Curve VETgirl blog Chris Kennedy

Figure 1: Idealized version of three cardiac function curves. The green curve represents normal (baseline) contractility. The red curve represents increased contractility. The purple curve represents decreased contractility. Note that the stroke volume changes with increases and decreases in contractility despite an unchanged preload (dotted lines). Drawing courtesy of Dr. Christopher Kennedy, DACVECC, DECVECC

When we use FCU to evaluate LV systolic contraction, we are not evaluating cardiac performance nor are we assessing contractility. We are assessing the LV’s contraction during systole, given the loading conditions (preload and afterload) and its intrinsic contractility (unmeasurable), which we can call “contractile function” or “systolic function.”

We can use systolic function to help us understand a case. Again, it is all about clinical integration. Mean arterial pressure (MAP) is the product of CO and systemic vascular resistance.(3)  CO is the product of SV and heart rate.(3)  SV is the difference between the volume of blood in the heart at end-diastole and end-systole: as the SV is generated during the ejection phase, the LV lumen reduces and we see this reduction as contraction. So, if the MAP is low and the systolic function via FCU is decreased, the cause of the hypotension may be decreased systolic function.

Two exceptions highlight the limitation of FCU systolic function assessments. Firstly, we recall that the systolic function does not accurately describe SV: while we may obtain an idea of the relative change in blood volume in the heart between diastole and systole, we do not know the absolute change. Dogs with dilated cardiomyopathy may be compensated: the systolic function may look decreased, but the patient’s cardiac performance is sufficient.(4)  This occurs as the relative change in volume from end-diastole to end-systole is decreased but the absolute change (i.e., the stroke volume) is sufficient. Cardiac performance (the sufficiency of cardiac output) is therefore a clinical assessment, not an echocardiographic assessment.

Secondly, in cases such as sepsis, the systolic function may seem normal or even increased, though there can be myocardial dysfunction that we do not appreciate with FCU.(5,6)  Our poor ability to detect myocardial dysfunction occurs, in part, due to decreased afterload (vasodilation). Decreased afterload increases the apparent contractile function. However, we cannot assess intrinsic contractility, which may be decreased in sepsis.(5,6)  Cardiac performance (measured as CO) may or may not be sufficient, though vascular performance (the perfusion pressure within the arterial system to meet metabolic needs) is insufficient in the hypotensive septic patient. Systolic function can change with interventions – fluids, diuretics, vasopressors, or inotropes – which highlights the role of regular FCU monitoring and ideally formal echocardiography by a cardiologist in these complex cases.

So, what does assessment of systolic function via FCU tell us? It tells us, given the loading conditions, the intrinsic contractility and the heart rate, how the left ventricle is contracting now – an instantaneous assessment of LV systolic function. If the loading conditions, contractility or heart rate change, the LV systolic function may also change.

References and further reading
1. Muir WW, Hamlin RL. Myocardial Contractility: Historical and Contemporary Considerations. Front Physiol. 2020 Mar 31;11:222. doi: 10.3389/fphys.2020.00222.
4. Myocardial diseases of the dog. In: Cardiovascular Disease in Companion Animals Dog, Cat, and Horse. Ware WA and Bonagura JD (editors), 2nd edition. Boca Raton, Florida, USA; pp. 607 – 624.
5. Habimana R, Choi I, Cho HJ, Kim D, Lee K, Jeong I. Sepsis-induced cardiac dysfunction: a review of pathophysiology. Acute Crit Care. 2020 May;35(2):57-66. doi: 10.4266/acc.2020.00248.
6. Boissier F, Aissaoui N. Septic cardiomyopathy: Diagnosis and management. J Intensive Med. 2021 Dec 27;2(1):8-16. doi: 10.1016/j.jointm.2021.11.004.

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